Outcome analysis of carotid artery occlusion.

The outcome of carotid artery occlusion was studied through the retrospective identification of 115 affected patients. The majority were white (77%) males (61%) with multiple atherogenic risk factors and suffering ipsilateral stroke (57%). Those patients presenting with stroke were not distinguished by demographic features, risk factors, lipid profile, medical regimen, or subsequent mortality when compared with those without. Overall, 36 patients (31%) required contralateral carotid endarterectomy (CEA), with one (2.8%) perioperative stroke, whereas 4 (3%) underwent ipsilateral external CEA without incident. With 81% follow-up (mean 3.9 years), the overall mortality of the group was 46%; the annualized risk of ipsilateral stroke was 1.6%. This study documents a significant risk of stroke and contralateral occlusive disease with ipsilateral carotid artery occlusion, which cannot be reliably predicted by clinical criteria. Duplex surveillance is valuable, but flow velocity measurements alone may be misleading. Surgical endarterectomy can be performed with an acceptable rate of perioperative stroke.

Primary intimal sarcoma of the aorta associated with a dacron graft and resulting in arterial rupture.

Primary arterial neoplasms are rare lesions which have been most frequently associated with local or constitutional symptomatology, and with distal embolization. Perirenal aortic disruption with pseudoaneurysm formation due to an intimal sarcoma adjacent to a previously placed prosthetic graft is reported in a 66-year-old man. This case supports the premise that the presence of a vascular prosthesis might result in the induction of an arterial wall malignancy. This should be considered when an intraluminal mass is identified in the absence of other arterial pathology. Although the prognosis of these tumors is poor, their preoperative recognition may enhance treatment outcomes.

The influence of platelet-smooth muscle cell interaction on the oxidative modification of low-density lipoprotein.

OBJECTIVE: In view of the recognized association between thrombosis and atherosclerosis, it is hypothesized that exposure of arterial smooth muscle cells (SMC) to thrombogenic agents such as platelets and thrombin will alter the oxidation of low-density lipoprotein (LDL) and that this effect may be diminished by thrombin inhibition. METHODS: Quiescent human aortic SMC in culture were exposed to LDL (40 microg protein/ml) alone or with washed human platelets (5 x 10(6)/ml), thrombin (40 units/ml), or a combination of these agents for 48 h. The media were removed, and both media and cell lysate fractions were assayed for malondialdehyde (MDA) content as an index of oxidation. Isolated platelets exposed to LDL and thrombin were studied in a similar manner to determine their individual oxidative activity. Finally, SMC and platelets were incubated with LDL and varying concentrations of thrombin (10-80 units/ml), both alone and in the presence of the thrombin inhibitors hirudin (u/u), and heparin (u/u), and MDA was measured. RESULTS: SMC and platelets each demonstrated an ability to oxidize LDL, increasing MDA concentrations by 1.8- (P < 0.05) and 4- (P < 0.01) fold, respectively, compared to lipid-free media. Both platelets (P < 0.05) and thrombin (P < 0.001) enhanced the oxidation of LDL by SMC, while a combination of these two agents resulted in an additive effect (P < 0.001). The SMC lysate fraction showed an increase in oxidative products following exposure to platelets (P < 0.01) but not thrombin, suggesting that platelets stimulated uptake of the oxidized lipid by the SMC. Isolated platelets responded to thrombin with an increase in MDA within the media (P < 0.001). Smooth muscle cells exposed to thrombin also showed a dose-dependent increase in LDL oxidation (P < 0.01). This effect was not altered by hirudin, but was significantly inhibited by heparin (P < 0.05). CONCLUSIONS: These results indicate that the oxidative potential of SMC and platelets is enhanced by their coincubation and by their concurrent exposure to thrombin. Heparin appears to block thrombin-stimulated oxidation. This interaction could be relevant to the dynamic interaction between atherosclerosis and thrombogenesis.